首页 文献索引 SCI期刊 AI助手
条件筛选
相关性 最新发表 最早发表
全文 标题 期刊 作者
Clinical Trial Case Reports Meta-Analysis RCT Review Systematic Review
Classical Article Case Reports Clinical Study Clinical Trial Clinical Trial Protocol Comment Comparative Study Editorial Guideline Letter Meta-Analysis Multicenter Study Observational Study Randomized Controlled Trial Review Systematic Review
模糊 精准
{{tag.shortname||tag.name}}:{{getFilterLabel(field)}} Clear All
Hai Chen,Jingmin Shu,Rekha Mudappathi et al. Hai Chen et al.
Intratumor heterogeneity arises from ongoing somatic evolution complicating cancer diagnosis, prognosis, and treatment. Here we present TEATIME (es t imating e volution a ry events t hrough s i ngle-ti m epoint s e quencing), a novel comput...
Edmond M Kwan,Alexander W Wyatt Edmond M Kwan
Given the potential for cooccurrence of multiple AR genomic alterations in the same or competing subclones of a patient, it is distinctly challenging to attribute blanket clinical significance to any individual alteration.
Felix Horns,Christopher Vollmers,Cornelia L Dekker et al. Felix Horns et al.
Antibodies are created and refined by somatic evolution in B cell populations, which endows the human immune system with the ability to recognize and eliminate diverse pathogens. However, the evolutionary processes that sculpt antibody repe...
Gunes Gundem,Peter Van Loo,Barbara Kremeyer et al. Gunes Gundem et al.
Cancers emerge from an ongoing Darwinian evolutionary process, often leading to multiple competing subclones within a single primary tumour. This evolutionary process culminates in the formation of metastases, which is the cause of 90% of cancer-related deaths.
Lucia Flossbach,Karlheinz Holzmann,Torsten Mattfeldt et al. Lucia Flossbach et al.
We found genomic heterogeneity in both cases, supporting the theory of competing subclones in the evolution and progression of extranodal marginal zone B-cell lymphoma. Copyright © 2012 UICC.
Moritz Gerstung,Christian Beisel,Markus Rechsteiner et al. Moritz Gerstung et al.
According to the clonal evolution model, tumour growth is driven by competing subclones in somatically evolving cancer cell populations, which gives rise to genetically heterogeneous tumours.
Jonathan J Keats,Marta Chesi,Jan B Egan et al. Jonathan J Keats et al.
A detailed analysis of one high-risk patient sampled at 7 time points over the entire disease course identified 2 competing subclones that alternate in a back and forth manner for dominance with therapy until one clone underwent a dramatic linear evolution.